SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Psychogenic polydipsia can occur in infants and may be associated with urinary tract dilation. It is not known whether this dilation can lead to a decline in renal function, as has been reported in patients with diabetes insipidus and hydronephrosis. The structural changes may be reversed by treatment of polydipsia through fluid restriction and counseling.
The case of a 17 year-old female with psychogenic polydipsia is reported; 13 out of 18 members of her maternal family were known to have had polydipsia and polyuria, but only two had undergone endocrine investigations--one had diabetes insipidus and one also had psychogenic polydipsia. There are probable contributions of non-genetic family factors including imitation and identification to the development of this patient's condition. Detailed family and developmental histories may be of particular assistance in the understanding of the psychogenesis of the disorder in some patients.
The role of the renin-angiotensin system in polyuric patients was studied in 5 patients with pituitary diabetes insipidus, 1 patient with nephrogenic diabetes insipidus and 3 patients with psychogenic polydipsia by determining the plasma renin activity and infusing an angiotensin II analog, 1-Sar, 8-Ile angiotensin II. In all patients with diabetes insipidus, plasma renin activity was markedly increased and the blood pressure was reduced in 5 of 6 patients by the administration of the angiotensin II analog. In the other patient, the blood pressure remained unchanged. The plasma renin activity and response of blood pressure to the angiotensin II analog in a patient with nephrogenic diabetes insipidus were not significantly different from there of patients with pituitary diabetes insipidus. On the other hand, in all patients with psychogenic polydipsia, plasma renin activity was normal or low, and the blood pressure increased with the administration of the angiotensin II analog. These results suggest that evaluation of the renin-angiotensin system by determining plasma renin activity and infusing an angiotensin II analog is useful in differentiating between diabetes insipidus and psychogenic polydipsia.
A case of psychogenic polydipsia is presented that showed psychic decompensation and compulsive drinking under the acute stress of an imminent operation for ovarian cyst. Without any indication of an underlying organic disease process the patient developed acute water intoxication due to the uncontrolled intake of water from the tap, this caused hyponatremia, brain edema, coma and status epilepticus. The physiology of water intoxication is reviewed in relation to this case, which is also remarkable for the acute onset and the shortness of the polydipsic state.
OBJECTIVE: To report a case of rhabdomyolysis related to correction of hyponatremia secondary to psychogenic polydipsia, possibly complicated by the use of ziprasidone. CASE SUMMARY: A 50-year-old white man treated for 3 weeks with ziprasidone 40 mg twice daily for chronic paranoid schizophrenia was admitted to the intensive care unit after a witnessed generalized seizure. Marked hypotonic hyponatremia was present secondary to psychogenic polydipsia. After correction of hyponatremia with intravenous NaCl 0.9%, he developed a substantial elevation in the creatine kinase level without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome. Renal failure or compartment syndrome did not complicate the clinical picture. DISCUSSION: It is well known that severe hyponatremia can cause neurologic complications such as stupor, seizures, and even coma. Hyponatremia from water intoxication (n = 28) and its correction with intravenous fluids (n = 2) may cause non-neurologic complications such as rhabdomyolysis. An explanation may lie within the calcium-sodium exchange mechanism across the skeletal myocyte or the failure of cell volume regulation secondary to extracellular hypo-osmolality. Neuroleptic medications have been linked to the development of rhabdomyolysis, with antipsychotics being the primary offenders. As of August 2005, there has been only one reported case of rhabdomyolysis related to correction of hyponatremia complicated by an atypical antipsychotic (clozapine). It is possible that ziprasidone, like clozapine, may enhance muscle cell permeability leading to rhabdomyolysis under similar conditions. CONCLUSIONS: Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications.
This report describes the behavioral treatment of psychogenic polydipsia in an autistic, severely mentally retarded woman who had a history of self-induced water intoxication. Treatment emphasized the use of edibles and reductions in activity demands to reward water refusal. Employing this procedure, paraprofessional staff normalized the client's water consumption, and thereby prevented further episodes of potentially-fatal water intoxication.
Psychiatric patients presenting with chronic psychogenic polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacologic intervention was attempted in three patients and was successful in one. One patient had a significant and sustained reduction of water intake while on 160 mg of propranolol. One patient did not improve with either propranolol or captopril while a third patient showed no improvement of serum sodium with demeclocycline nor reduction of water intake with propranolol. The potential mechanisms by which these pharmacologic agents might alter thirst in patients with primary polydipsia are discussed.
The term "water intoxication" is used to describe a condition of agitation, delirium, convulsion, and coma brought on by excessive intake of water, resulting in severe hyponatremia. Psychogenic polydipsia (compulsive water drinking) has until recently been considered a relatively benign process. Since 1974, however, three fatal cases of water intoxication, resulting from psychogenic polydipsia, have been reported. All three individuals died while hospitalized, thereby permitting performance of blood electrolyte determinations and documentation of the associated electrolyte imbalance. In the authors' case, there was a well-documented prior episode of water intoxication in which serum electrolytes showed a pattern typical of this entity. Death, however, occurred at home, thus preventing valid serum electrolyte determinations to be performed. Analysis of the vitreous humor revealed a severe hyponatremia, thus substantiating the diagnosis of fatal water intoxication. This case, once again, points out the usefulness of electrolyte analyses on the vitreous humor as an aid to establishing a cause of death.
Psychogenic polydipsia (PPD), which can lead to water intoxication (WI), is a problem with many psychiatric patients. The case history of one schizophrenic patient presented here shows that propanolol therapy can reduce PPD and WI, possibly decrease thirst, and improve schizophrenic symptoms and behavior. When combined with regular weight evaluation and behavioral treatment to restrict water intake, the therapy can further reduce the risk of developing life-threatening WI complications.
A rhesus monkey developed psychogenic polydipsia after a change in feeding regimen was instituted. Hyposthenuria, hyponatremia, hypochloremia, and an abnormal calculated plasma osmolality were found. Water deprivation testing and administration of antidiuretic hormone indicated that renal medullary solute depletion had resulted from the prolonged polyuria. Restricted water consumption resulted in resolution of the electrolyte abnormalities and restored ability to excrete concentrated urine.
A 50-year-old Japanese man had been suffering from polydipsia and polyuria for 2 months without any other specific symptoms. His daily urinary output reached 5 liters. On admission, no abnormalities of the kidneys, heart, thyroid, adrenals, pituitary or hypothalamus were detected by laboratory tests and MRI of the head. Pure psychogenic polydipsia was ruled out because his urine volume did not decrease sufficiently with 18 h of water deprivation and the subsequent injection of aqueous vasopressin. Plasma arginine vasopressin (AVP) levels against plasma osmolality remained within the normal range during the test. These results indicated that diabetes insipidus in this case was caused by renal insensitivity to AVP. The symptoms disappeared spontaneously, and marked improvement was observed in a second water deprivation test 1 month later, although the maximum urine concentration was still subnormal. The combination of both latent insufficiency of AVP secretion and impairment of the renal countercurrent system induced by psychogenic polydipsia was speculated as a possible mechanism for the transient nephrogenic diabetes insipidus in this case.
A case of psychogenic polydipsia is presented. A 40 year old female was brought to the emergency room after a sudden seizure at home. The patient had spontaneous eye opening, was making incomprehensible sounds and had abnormal and agitated flexion of the limbs. Severe cerebral edema was seen on the computed tomogram. The patient was found to have hypotonic polyuria and hyponatremia. Two months previously, the patient had stopped taking bromazepam (a benzodiazepine) and on the advice of a neighbour had taken plenty of water to avoid withdrawal symptoms. The diagnosis and therapy are discussed.
Of 10 patients who excreted urine with low specific gravity and had chronic psychogenic polydipsia, five had urinary tract abnormalities, ranging from large bladders with large postvoid residuals to severe hydronephrosis, renal back pressure atrophy, and renal failure.
Three infants with symptoms of diabetes insipidus are described. Psychogenic polydipsia, which rarely occurs in infancy, was diagnosed. It was caused by mistakes made by the parents in bringing up these children.
Severe neurologic complications resulting from correction of hyponatremia are common, but reports of nonneurologic sequelae are scarce. This article describes a patient in whom rhabdomyolysis developed during correction of severe hyponatremia attributable to psychogenic polydipsia. Relevant material about volume regulation in the cell is presented, and a potential mechanism of cell damage is proposed. This case report emphasizes the importance of monitoring for nonneurologic complications during correction of hyponatremia.
Congenital renal dysplasia was tentatively diagnosed, based on ultrasound and an intravenous urogram, in a 5-month-old female with polyuria and polydipsia. Creatinine clearance measurement revealed that the renal dysplasia was not the cause of the polyuria. A modified water deprivation test eliminated other differential diagnoses and confirmed psychogenic polydipsia.